Impacts of lobetyolin on the proliferation,apoptosis and epithelial-mesenchymal transformation of gastric cancer cells by regulating the AKT/GSK-3β/snail signaling pathway
Objective To investigate the impacts of lobetyolin(LOB)on the proliferation,apoptosis and epithelial-mesenchymal transformation(EMT)of gastric cancer(GC)cells by regulating the protein kinase B(AKT)/glycogen synthase kinase 3β(GSK-3β)/Snail signaling pathway.Methods The GC cell line SGC7901 was induced with blank control,low-dose LOB(10μmol/L LOB),medium-dose LOB(20μmol/L LOB),high-dose LOB(40μmol/L LOB)and high-dose LOB + SC79(40μmol/L LOB + AKT activator SC79 20μmol/L).Cell proliferation,migration and invasion were detected by CCK-8,wound healing and Transwell assay,respectively.The mRNA levels of AKT,GSK-3β,and snail1 were detected by Reverse transcription quantitative real-time polymerase chain reaction(RT-qPCR).Protein expressions of key proteins in the AKT/GSK-3β/snail signaling pathway and those associated with apoptosis and EMT were detected by Western blot.Results The optical density at 450nm(OD450)value at 48h and 72h,wound healing rate,invasive cell number,mRNA levels of AKT,GSK-3β and snail1 and protein levels of AKT,phosphorylated GSK-3β,snail1,Bcl-2,N-cadherin and Vimentin were significantly lower in SGC7901 cells induced with medium-dose and high-dose LOB than those induced with blank control(P<0.05),while the apoptotic rate and protein expressions of Bax and E-cadherin were significantly higher(P<0.05).The treatment of SC79 weakened the inhibitory effect of LOB on the proliferation and EMT of GC cells,and inhibited cell apoptosis.Conclusion LOB may inhibit the proliferation and EMT process of GC cells and promote cell apoptosis by inhibiting the AKT/GSK-3β/snail signal pathway.
lobetyolinprotein kinase B/glycogen synthase kinase-3β/Snail signal pathwaygastric cancerepithelial-mesenchymal transformation
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